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We have studied synaptic function in a transgenic mouse strain relevant to Alzheimer's disease (AD), overexpressing the 695 amino acid isoform of human amyloid precursor protein with K670N and M671L mutations (APP695SWE mice), which is associated with early-onset familial AD. Aged-transgenic mice had substantially elevated levels of Aβ (up to 22 μmol/gm) and displayed characteristic Aβ plaques. Hippocampal slices from 12-month-old APP695SWE transgenic animals displayed reduced levels of synaptic transmission in the CA1 region when compared with wild-type littermate controls. Inclusion of the ionotropic glutamate receptor antagonist kynurenate during preparation of brain slices abolished this deficit. At 18 months of age, a selective deficit in basal synaptic transmission was observed in the CA1 region despite treatment with kynurenate. Paired-pulse facilitation and long-term potentiation (LTP) were normal in APP695SWE transgenic mice at both 12 and 18 months of age. Thus, although aged APP695SWE transgenic mice have greatly elevated levels of Aβ protein, increased numbers of plaques, and reduced basal synaptic transmission, LTP can still be induced and expressed normally. We conclude that increased susceptibility to excitotoxicity rather than a specific effect on LTP is the primary cause of cognitive deficits in APP695SWE mice.

the journal of neuroscience/the journal of neuroscience

Age-Related Impairment of Synaptic Transmission But Normal Long-Term Potentiation in Transgenic Mice that Overexpress the Human APP695SWE Mutant Form of Amyloid Precursor Protein